CREB1 may not play major role in the pathophysiology of Alzheimer's disease in Han Chinese.

Our results provide evidence that SETD2 and CREB1 contribute to cisplatin cytotoxicity in non-small cell lung cancer via regulation of the ERK signaling pathway, and their inactivation may lead to cisplatin resistance

High CREB1 expression is associated with Neuroblastoma.

This study demonstrates that the presence of rs928413(G) allele in the IL33 promoter results in its increased activity in a human lung carcinoma cell line due to binding of the cAMP (cyclic adenosine monophosphate) response element binding protein 1 (CREB1) transcription factor. The results offer a tentative explanation for the negative effect of rs928413 on asthma development.

findings illustrate the significance of CREB-KDM4B-STAT3 signaling cascade in DNA damage response, and highlight that KDM4B may potentially be a novel oncotarget for colorectal cancer radiotherapy.

experiments mainly reveal that the CREB1 could affect glucose transport in glioma cells by regulating the expression of GLUT1, which controlled the metabolism of glioma and affected the progression of glioma.

These data highlight a novel arrestin-mediated modulation of CREB signalling, suggesting a reciprocal relationship between arrestin2 and arrestin3, wherein recruitment of arrestin3 restricts the ability of beta2AR to activate prolonged CREB phosphorylation by precluding recruitment of an arrestin2/Src/p38 complex.

The authors conclude that taurodeoxycholic acid-induced DNA damage may depend on the activation of TGR5, CREB and NOX5-S. It is possible that in Barrett's patients bile acids may activate NOX5-S and increase reactive oxygen species (ROS) production via activation of TGR5 and CREB. NOX5-S-derived ROS may cause DNA damage, thereby contributing to the progression from Barrett's esophagus to esophageal adenocarcinoma.

The mechanism of CBP-CREB association via their pKID/KIX domains studied by molecular dynamics free energy simulations has been reported.

The key findings of the present study demonstrated that CREB1 gene silencing results in aggravated vascular dementia that occurs as a result of inhibiting the PKA-CREB signaling pathway, thus exasperating cognitive dysfunction.

Data show that cAMP-response-element binding protein (CREB) is a central molecular node in the circuit responses after stroke that lead to recovery from motor deficits.

Creb1/Crtc1-3 and Sec14l3 could be important for early responses of the bronchial epithelium to Th2-stimuli.

These findings suggest that dendritic region-specific morphological changes in CA1 neurons by constitutive activation of CREB may contribute to improved learning and STM.

this study shows that CREB is a critical regulator of dendritic cells during the germinal center response

FXR exerts its function in L cells through interacting with CREB, a crucial transcriptional regulator of cAMP-CREB signaling pathway, to inhibit its transcriptional activity. Targeting FXR to rescue GLP-1 secretion may be a promising strategy for type II diabetes.

Unexpectedly, although dispensable for FOXP3 expression and for the homeostasis and suppressive function of thymus-derived Treg cells, CREB negatively regulates the survival of TGF-beta-induced Treg cells, and deletion of CREB resulted in increased FOXP3+ Treg cells in the intestine and protection in a colitis model

The absence of gut microbiota from birth was shown to be associated with decreased CREB expression, followed by decreases of protein kinase C beta (PRKCB) and AMPA receptors expression, and an increase of phosphorylation CREB (pCREB) expression.

Significant CREB activation in almost the whole amygdala and hippocampus was observed after unconditioned stimulus-retrieval, but conditioned stimulus-retrieval only stimulated CREB activation in the lateral amygdala and the CA3 of hippocampus. In addition, propranolol, a beta-adrenergic receptor antagonist, treatment suppressed memory retrieval-induced CREB activation.

We found several conserved cis elements in the frog CRF genes including a cAMP response element (CRE), activator protein 1 binding sites, and glucocorticoid response elements

p38 MAPK and CREB function along the dorsal-ventral axis in mesoderm patterning. The phosphorylated form of CREB (S133) is distributed in a gradient along the dorsal-ventral mesoderm axis and the p38 MAPK pathway mediates the phosphorylation of CREB.

CREB1 profil antigène

Antigen Summary

This gene encodes a transcription factor that is a member of the leucine zipper family of DNA binding proteins. This protein binds as a homodimer to the cAMP-responsive element, an octameric palindrome. The protein is phosphorylated by several protein kinases, and induces transcription of genes in response to hormonal stimulation of the cAMP pathway. Alternate splicing of this gene results in two transcript variants encoding different isoforms.